Editor's Note: Naive B cells are immune system cells that have not been exposed to an antigen, that is, they have not "learned" to identify an invader. Plasmablasts perform a similar function. Transitional B cells are cells that have not yet been transformed into different classes of immune cells. A large proportion of immature B cells leads to a decrease in a person's ability to combat previously encountered pathogens (humoral immunity). A shift toward increased numbers of immature B cells is found in autoimmune disease, such as lupus.
~Source: Clinical & Experimental Immunology, April 2013
By A. S. Bradley et al.
Summary
Chronic fatigue syndrome (CFS) is a heterogeneous disorder of unknown aetiology characterized by disabling fatigue, headaches, sleep disturbance and several other symptoms. The onset of CFS may follow a viral infection or period of stress. Patients with CFS do not have hypogammaglobulinaemia, predisposition to recurrent bacterial infections or symptoms of autoimmunity. To date, defects in B cell numbers or function have not been shown in the literature. However, treatment with anti-B cell therapy using Rituximab has recently shown benefit to CFS patients. We therefore postulated that patients with CFS had a subtle humoral immune dysfunction, and performed extended B cell immunophenotyping. We undertook a detailed characterization of the proportions of the different B cell subsets in 33 patients with CFS fulfilling the Canadian and Fukada criteria for CFS and compared these with 24 age- and gender-matched healthy controls (HC). CFS patients had greater numbers of naive B cells as a percentage of lymphocytes: 6.3 versus 3.9% in HC (P = 0.034), greater numbers of naive B cells as a percentage of B cells: 65 versus 47% in controls (P = 0.003), greater numbers of transitional B cells: 1.8 versus 0.8% in controls (P = 0.025) and reduced numbers of plasmablasts: 0.5 versus 0.9% in controls (P = 0.013). While the cause of these changes is unclear, we speculate whether they may suggest a subtle tendency to autoimmunity.
Source: Clinical & Experimental Immunology, Volume 172, Issue 1, pages 73–80, April 2013 A. S. Bradley, B. Ford, A. S. Bansal.
